The first objective of this thesis was to assess the feasibility of designing a “smart” degradable polymer that can release anti-inflammatory drugs in response to inflammatory-related enzymes. The drug polymer was synthesized using diisocyanates, poly(caprolactone)diols, and oxaceprol (OC) biomonomers. Biodegradation studies demonstrated that the trimethylhexamethylene diisocyanate-based drug polymer responded to an inflammatory enzyme to release more OC, while a 1, 12-diisocyanatododecane analog demonstrated minimal drug release. The drug delivery response was believed to be a direct function of the molecular structure and distribution of the hard segment. The second objective of this thesis was to elucidate the anti-inflammatory mechanisms of OC by investigating its effects on cytokine-induced monocytic-cells adhesion in human umbilical vein endothelial cells (HUVECs) in vitro. Results showed that OC had no direct effect on the monocyte-endothelium adhesion, suggesting that OC may mediate inflammation by mechanisms other than those suggested by the literature.

The first objective of this thesis was to assess the feasibility of designing a “smart” degradable polymer that can release anti-inflammatory drugs in response to inflammatory-related enzymes. The drug polymer was synthesized using diisocyanates, poly(caprolactone)diols, and oxaceprol (OC) biomonomers. Biodegradation studies demonstrated that the trimethylhexamethylene diisocyanate-based drug polymer responded to an inflammatory enzyme to release more OC, while a 1, 12-diisocyanatododecane analog demonstrated minimal drug release. The drug delivery response was believed to be a direct function of the molecular structure and distribution of the hard segment. The second objective of this thesis was to elucidate the anti-inflammatory mechanisms of OC by investigating its effects on cytokine-induced monocytic-cells adhesion in human umbilical vein endothelial cells (HUVECs) in vitro. Results showed that OC had no direct effect on the monocyte-endothelium adhesion, suggesting that OC may mediate inflammation by mechanisms other than those suggested by the literature.